成本核算在医院管理中的应用和进展

目前,我国医疗总费用的增长速度大大超过了国民经济和财政收入的增长速度[1]。卫生经费投入不足,药费居高不下,政府、企业不堪重负,医疗制度改革势在必行。成本核算是医院经济管理的基础工作,核算工作的深度和层次直接影响医院成本管理的成效。1医疗成本核算的概念医疗成本是卫生服务过程中所发生的物化劳动和活劳动耗费的总和。它由以下6大类成本构成:劳务费、业务费、公务费、原材料费、固定资产折旧费和管理费。医疗成本核算是按照《医院财务制度》有关成本费用开支范围的规定,核算医院在医疗服务过程中所支出的物质消耗、劳务报酬以及有…     

经尿道等离子双极汽化电切(TUPKVP)治疗前列腺增生症580例

目的:探讨经尿道等离子前列腺双极汽化电切术(TUPKVP)治疗前列腺增生的效果。方法:回顾性分析580例良性前列腺增生(BPH)患者行TUPKVP的临床资料。结果:中转开放手术2例,切除前列腺组织10~80 g,平均32.5 g。手术时间25~150 min,平均60 min,术中输血10例,无电切综合征(TURS)发生。术后随访2~36个月,患者最大尿流率升高,IPSS症状评分值降低,排尿通畅,疗效好,并发症少。结论:TUPKVP出血少,手术安全,疗效确切,是治疗前列腺增生的有效方法。     

Interactions between membrane IgM and the cytoskeleton involve the cytoplasmic domain of the immunoglobulin receptor

Cross-linking induced interactions between the membrane form of immunoglobulin (mIg) and the cytoskeletal matrix have been described by several groups. To date, the function of mIgM association with the cytoskeleton is not yet understood. Delineation of the molecular basis of these interactions will be instrumental in elucidating their function. We have previously shown that the Igα/β heterodimer is not required for ligand-induced mIgM binding to the cytoskeleton. In this study, we have investigated the role of other B cell-specific proteins in mediating these interactions. For this, we expressed mIgM in the non-hematopoietic human cervical carcinoma cell line HeLa S3 and verified the capacity of the surface-expressed IgM to interact with the cytoskeletal matrix upon cross-linking with anti-μ chain antibodies. We show here that only the mIgM molecule itself and no other B cell-specific protein(s) is required in mediating mIgM interactions with actin filaments. In an attempt to determine the cytoskeleton-binding site of mIgM we investigated the role of the cytoplasmic tail of mIgM (KVK) in binding the receptor to actin-based microfilaments. Using mutated forms of mIgM expressed in J558L cells, we show here that KVK plays a role in mediating these interactions. The absence of KVK did not, however, completely abrogate mIgM-cytoskeletal interactions, suggesting that there are additional molecular requirements for the ligand-induced mIgM binding to the cytoskeletal matrix.     

肾移植2,3,5年患者的免疫抑制用药分析

目的：分析肾移植后免疫抑制剂对长期存活的影响，寻找移植后不同时间合适的免疫抑制用药方案及其用药剂量。 方法：对肾移植一年以上、肾功能正常的４９７例患者进行５年连续随访。根据移植后２、３、５年的不同免疫抑制用药将患者分为三联、二联、传统二联治疗三组。统计各组的排异发生率，排异和无排异患者免疫抑制用药的种类、剂量及ＣｓＡ浓度，对排异患者追踪排异发生前１２个月内的药物更动情况。 结果：肾移植后２、３、５     

Involvement of NMDA and NonNMDA Receptors in Motor Task--related Activity in the Primary and Secondary Cortical Motor Areas of the Monkey

The involvement of the NMDA and non-NMDA receptors in the task-relatedneuronal activity of the primary motor cortex (MI), premotorcortex (PM), supplementary motor area (SMA), and an area rostralto the SMA (pre-SMA) of two monkeys (Macace fuscata) was examinedduring performance of a trained motor task. The selective NMDAantagonist 0-2-amino-5-phosphonovaleric acid (APV) and the non-NMDAantagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) wereiontophoretically applied to motor task-related neurons. A totalof 568 task-related neurons (435 movement related, 83 set related,50 mixed type) were recorded from the MI, PM, SMA, and pre-SMA,and the effects of APV and CNQX were examined in the individualneurons. In many neurons, APV selectively or preferentiallysuppressed the spontaneous discharge rather than movement-relatedactivity. In many neurons, the movement-related activity wasmore selectively or effectively suppressed by CNQX than by APV.However, the set-related activity was affected by both APV endCNQX. The neurons in layers I and II were affected more stronglyby APV end CNQX than those in layers V and VI. No correlationwas found between the magnitude of task-related activity inthe control (no drug application) period and the effectivenessof APV or CNOX. These results indicate that both NMDA and non-NMDAglutamate receptors are involved in motor task-related neuronalactivity of both primary and secondary motor areas, althoughthe contribution of these two receptors to individual neuronalactivity varies a great deal.     

Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs

We investigated the relative effects of 0.5, 1.0, 1.5, 2.0 MAC halothane and enflurane, and concurrent noxious stimulus on hepatic blood flow and oxygen consumption in 14 mongrel dogs randomly divided into groups of seven each. Hepatic arterial and portal venous blood flow (HABF and PVBF, respectively) were measured continuously using ultrasonic transit time flow meter. Mean arterial blood pressure (MAP), cardiac index (CI), hepatic oxygen supply, and hepatic oxygen consumption (H _{O 2}) were measured. Halothane significantly deceased HABF, but not PVBF in a dose dependent manner. Enflurane did not affect HABF and PVBF significantly. MAP and CI decreased in both groups, with halothane producing more marked decreases than enflurane. H _{O 2} did not change with enflurane, but did with halothane, producing significant differences, with halothane being greater at 1.5, 2.0 MAC. A noxious stimulus only caused minor change in blood flow. The results suggest that liver blood flow and oxygen consumption are affected differently by halothane and enflurane and that halothane has a stronger tendency to cause an imbalance between liver oxygen supply and consumption than dose enflurane.(Masaki E, Yasuda N, Tanifuji Y et al.: Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs. J Anesth 3: 118–122, 1989)     

Bcl11b is required for differentiation and survival of alphabeta T lymphocytes

The gene Bcl11b, which encodes zinc finger proteins, and its paralog, Bcl11a, are associated with immune-system malignancies. We have generated Bcl11b-deficient mice that show a block at the CD4-CD8- double-negative stage of thymocyte development without any impairment in cells of B- or gammadelta T cell lineages. The Bcl11b-/- thymocytes showed unsuccessful recombination of V(beta) to D(beta) and lacked the pre-T cell receptor (TCR) complex on the cell surface, owing to the absence of Tcrb mRNA expression. In addition, we saw profound apoptosis in the thymus of neonatal Bcl11b-/- mice. These results suggest that Bcl11b is a key regulator of both differentiation and survival during thymocyte development.